In the Western world, maculopathy or AMD is the leading cause of blindness in the elderly population and affects 10%-13% of adults over 65 in North America, Europe, Australia and Asia In 2012 the undiagnosed prevalence of AMD in the USA was estimated to be 2.3 million. Estimates of the global cost due to AMD are US$343 billion with US$255 billion in direct health care costs.
According to the International Classification age-related maculopathy (ARM) is a degenerative disease of the macula characterized in the early stage by large, soft yellow drusens, hyper-/hypopigmentation of the retinal pigment epithelium (RPE), and a moderate loss of central vision (age-related maculopathy). Age related maculopathy disease (AMD) is a late stage of ARM. Dry AMD refers to geographic atrophy and wet AMD is characterized by choroidal neovascularization (CNV), detachment of the RPE, subretinal hemorrhage or retinal scarring.
Currently, several AMD classification schemes, grading systems, and severity scales have been developed in an effort to provide standards to assist clinicians and researchers in the diagnosis and management of this important disorder. The most current clinical classification of AMD takes in consideration pigment abnormalities and is illustrated in FIG. 16.
It is believed the ultimate therapy for AMD will lie in the preclinical identification of those who are genetically “at risk” for the disease and treatment with genetically specific supplements. At the present time, AMD is initially diagnosed by an ophthalmologist or optometrist with a fundus examination and Amsler grid of patients who complain of a decrease in their vision. The hallmarks of early AMD are yellow drusens and pigment abnormalities (hypo and hyperpigmentation) of the retinal pigment epithelium (RPE) which occur after the onset of the AMD process. AMD is characterized by a degeneration of the retinal pigment epithelium and photoreceptors (rod and cones) and a thickening of the Bruch's membrane in the macula.
The early detection of AMR could reduce the growing societal burden by targeting and emphasizing modifiable habits earlier in life. With genetic testing antioxidants and other supplements specific to the patient's genotype can be recommended. More frequent examinations of those at high risk due to family history or signs of early or intermediate disease would be beneficial.
It is believed that the pigmentary changes observed in the macula of AMD eyes are attributable to degenerative changes in the highly melanized RPE cells because most of the early clinical signs and histopathological changes have been localized to this cell layer. It has been suggested that melanin in the retinal pigment epithelium (RPE) and choroid may protect the macular region by its antioxidant capability and its capability to attenuate or reflect light thereby decreasing photochemical light damage.
In retinoscopy, a light is shone into a patient's eye and the reflected “streak” of light is used to estimate the correction of a patient's refractive error. The results are then the beginning point for a refraction. However, with the calibrated retinoscope and this technique, the brightness of the reflected beam is dependent on the health of the pigment epithelium and thus gives an early indication of macular pathology. This calibrated diagnostic retinoscope and technique allow the general ophthalmic physician to detect early and late stages of the destruction of the retinal pigment epithelium in AMD. The common denominator between AMD and the pupillary reflex in retinoscopy lies in the melanin pigment particles of the microvilli of the retinal pigment epithelium (RPE) which surrounds the photoreceptors, the choroid and/or the outer segment of the cones.
In 1926, Jacob C Copeland designed a retinoscope (U.S. Pat. No. 3,597,051) and a technique of retinoscopy which has since been taught to optometrists and ophthalmologists for obtaining an objective measurement of the refractive error of patient's eyes for spectacles and/or contact lenses. All retinoscopes have been based upon on his work.
Originally, Copeland's and other retinoscopes used diverging light and spots of light to estimate the refractive error. Copeland introduced streak retinoscopy in the US and it was rapidly accepted because it made determination of the axis of astigmatism more precise. The technique was referred to as “streak retinoscopy” because a streak of reflected light, or the pupillary reflex, was produced during the technique.
In 1968, Copeland and Walter M. Lewis designed the Copeland Optec 360 Streak Retinoscope, U.S. Pat. No. 3,597,051 (as illustrated in FIG. 17). This retinoscope contains a +20.00 D condensing lens and a bi-pin filament bulb. When the thumb-slide is in its upper position, the filament of the lamp is less than five centimeters from the condensing lens and the rays emanating from the filament and passing out of the condensing lens are diverging. Moving the thumb-slide to a lower position causes the light rays to converge. When the filament is at the focal point of the +20.00 D lens or approximately 5 cm from the +20.00 D lens, the light rays are parallel.
Sims' calibrated refractive retinoscopic techniques uses converging rather than diverging light. The Sims' retinoscope can also be used for calibrated diverging or conventional diverging retinoscopic techniques. It has been modified so that auxiliary lenses can be attached to the back of the head of the retinoscope to place the examiner's eye in focus with the patient's pupillary plane in order to have an identical (conjugate) image of the pupillary reflex. Parallel light is used after the refractive error has been determined to judge the streak on a reflectance scale 1 (very poor and difuse) to 5 (brilliant).
In conventional retinoscopy, the pupillary reflex cannot be used to evaluate the melanin reflectance. The endpoint of conventional retinoscopy is an infinity neutrality reflex which fills the pupil and there is no streak. The width of the reflected retinoscopic light from the reflecting membrane spans an area much larger than the size of the pupil and is enormous, making it impossible to evaluate the reflectance of the macular pigment (MP). With conventional retinoscopy, the refractive error is initially determined by under correcting the refractive error to create a visible with-motion pupillary streak reflex that expands and moves at an exponentially increasing speed as neutrality is reached. These exponential changes of the with-motion streak makes it impossible to evaluate the reflectance of the MP.
Production of the Pupillary Reflex:
The cones act as an optical waveguide for visible light due to their tubular structure and the index gradient between the cell wall and internal medium. Since the cone's receptors are tightly packed, they act as a “fiber optic plate” extending from the external limiting membrane to the pigment epithelium (as illustrated in FIG. 18). Therefore light, that strikes the outer limiting membrane located at the openings of the photoreceptors, is transmitted to the photosensitive pigment in the outer segments by a waveguide mechanism and then reflected to the outer limiting membrane.
The reflected light from the retina pigment epithelium (RPE) interface appears to be due to Fresnel reflection from the melanin granules within the melanosomes in the RPE. A Fresnel reflection is a reflection of light on a planar interface between two homogeneous media having different refractive indices. The melanin granules in the pigment epithelium have a high index of refraction compared to the surrounding tissue. The reflected light then reenters the photoreceptors and transmitted to the external limiting membrane (ELM) and pupil. The ELM is considered the effective ocular reflecting surface for visible light in the performance of retinoscopy or photorefraction. Conventionally, the pupillary reflex is used to measure or estimate a refractive error, not to evaluate the reflectance from the melanin pigment.
Macular Degeneration and Reflectance:
Most of the early clinical signs and histopathological changes have been localized to the pigment epithelium. It is believed that it is the melanin in the retinal pigment epithelium (RPE) and choroid which protects the macular region through its antioxidant capability and its capability to attenuate blur light thereby decreasing photochemical light damage. Healthy pigment epithelium is more reflective than that which is damaged and when evaluated produces a brilliant to clear streak.
The calibrated retinoscope and diagnostic technique described in this patent application allows the average ophthalmic physician to detect early and late stages of the destruction of the retinal pigment epithelium in AMD.
The relevant prior art includes the following references:
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